Download Exercise tolerance in the heat on low and normal

Clinical Science ( 1989)76,553-557
553
Exercise tolerance in the heat on low and normal salt intakes
M. HARGREAVES", T. 0. MORGAN", R. SNOWt
AND
M. GUERINS
*Department of Physiology, University of Melbourne, Parkville, +Departmentof Physical Education and Recreation, Footscray Institute
of Technology, Footscray, and +Departmentof Biochemistry, Repatriation General Hospital, Heidelberg, Australia
(Received 6 June/22 August 1988; accepted 4 October 1988)
SUMMARY
1. Salt restriction is recommended in the treatment of
hypertension and is included in national dietary guidelines, but its effect on exercise in hot conditions has not
been extensively studied.
2. The effects of 2 weeks on two levels of salt intake
(50 and 150 mmol/day) on the ability to exercise (60% of
maximal oxygen uptake) in a. hot environment (35°C)
were studied in eight healthy normotensive subjects.
3. All subjects were able to complete the exercise load
on the two levels of salt intake. No differences in mean
oxygen uptake, heart rate or rectal temperature during
exercise were observed between the two salt intakes.
4. Plasma sodium, potassium and osmolality were
similar on the two salt intakes both before and during
exercise. Plasma renin activity and aldosterone concentration were elevated after 2 weeks on the reduced salt
intake and remained so during exercise.
5. The estimated sweat rate during exercise was
similar on the two salt intakes but the loss of sodium was
less on the low salt intake.
6. On the basis of these results it is concluded that
moderate salt restriction does not impair the ability to
exercise in a hot environment.
Key words: aldosterone, diet, exertion, renin, sodium
restriction.
Abbreviations: ANG I, angiotensin I; Vo, max., maximal
oxygen uptake.
INTRODUCTION
In recent years dietary salt restriction has been advocated
in the management of hypertension [ 1, 21. Restriction of
sodium intake has also been included in the nutritional
goals of a number of countries [3,4]. It has been suggested
that this approach may increase the risks associated with
the physiological stress of exercise, heat exposure or
Correspondence: Professor T.O. Morgan, Department of
Physiology, University of Melbourne, Parkville, 3052, Australia.
volume depletion [5, 61. Since regular exercise has also
been shown to lower blood pressure [7], and may be used
in combination with salt restriction [8], it is important to
determine whether individuals on a reduced salt intake
are at increased risk during exercise, especially when performed in a hot environment. Early work examining this
question [9] suggested that exercise-heat tolerance was
impaired on a 'low' salt intake (103 mmol/day) compared
with a 'moderate' intake (259 mmol/day). In contrast,
Armstrong et al. [lo]have demonstrated that the ability to
exercise in the heat on repeated days is unaffected by a
reduction in salt intake from 400 to 100 mmol/day. The
present study was undertaken to further examine the
effect of moderate salt restriction (50 mmol/day) on the
physiological responses to combined exercise and heat
stress.
METHODS
Eight male adults [23.4f 1.1 years, maximal oxygen
uptake ( vo, max.) = 4.05 k 0.24 I/&, mean fSEMI with
normal blood pressure (see Table 1)agreed to take part in
this study after being informed of the risks and stresses
associated with the protocol and having given written
consent. The study was approved by the ethics committees of the University of Melbourne and Footscray
Institute of Technology. The subjects were physically
active but were neither specifically trained nor heat
acclimatized, and were familiar with the exercise procedures used in the laboratory.
In consultation with a dietitian, subjects selected a
range of foods to produce a daily sodium intake of
approximately 50 mmol and maintained this diet for 4
weeks. For two 2-week periods subjects ingested either
slow sodium (Ciba-Geigy, 100 mmol/day; CON) or
placebo tablets (LOW), with a randomized, double-blind
cross-over design, so that sodium intakes of 150 and 50
mmol/day, respectively, would be obtained. Four subjects
received slow sodium tablets first; the remaining four
received placebo. Dietary adherence was checked by 24 h
urine collections on the last 2 days of each 2-week period.
At the end of each 2-week period exercise-heat tolerance
M. Hargreaves et al.
554
was assessed during 60 min of cycling exercise at a workload requiring approximately 60% of maximal oxygen
uptake ( Vo2max.), in a heat chamber maintained at 35°C
and 25% relative humidity. Subjects reported to the
laboratory on the morning of a trial after an overnight fast
and were weighed nude on a Sauter balance ( k5 g). A
thermistor probe (Yellow Springs Instrument) was
positioned to a depth of 10 cm to monitor rectal temperature. A catheter was inserted into a forearm vein and after
sitting quietly for 15-20 min the resting blood sample was
obtained. Subjects then entered the chamber and commenced exercise on a Monark bicycle ergometer. Heart
rates (cardiac auscultation) and rectal temperatures were
recorded every 10 min during exercise. Expired air was
collected in Douglas bags for oxygen uptake determination using Applied Electrochemistry oxygen and carbon
dioxide gas analysers and a Parkinson-Cowan gas meter,
calibrated against a Tissot spirometer. Venous blood
samples were obtained at 15, 30 and 60 min of exercise
and these, together with the resting sample, were analysed
for sodium, potassium, osmolality, plasma renin activity
and plasma aldosterone concentration. On completion of
the exercise subjects exited the chamber, sweat samples
were obtained using a washdown technique [ 111, and
post-exercise body weight was measured. No fluid was
ingested during exercise.
Blood for electrolytes, osmolality and aldosterone was
collected in chilled tubes containing a small amount of
lithium heparin; the tubes for plasma renin activity contained ethylenediaminetetra-acetate. These samples were
centrifuged and the plasma stored at -80°C until
analysis, except that for electrolytes which remained on
ice and was analysed later on the same day. Plasma
sodium and potassium were measured using indirect
reading ion-selective electrodes, while urine and sweat
samples were analysed by flame photometry. Osmolality
was measured on a vapour pressure osmometer (Wescor
Inc, Logan, UT, U.S.A.). Plasma renin activity (Biodata
Labs, Rome, Italy) and plasma aldosterone concentration
(Diagnostic Products Corporation, Los Angeles, CA,
U.S.A.) were measured by radioimmunoassay. On the day
before the exercise-heat tolerance test, maximal exercise
performance was assessed during a 30 s maximal effort
on an air-braked cycle ergometer (Repco, Melbourne,
Australia). Peak power and total work were obtained from
an Exertech work monitor unit, interfaced with the
ergometer.
The data from the two trials were compared using a
paired t-test and where appropriate analysis of variance
for repeated measures. The slopes of the aldosteronetime plots were obtained using linear regression analysis.
Data are reported as means fSEM.
RESULTS
All subjects successfully modified their dietary sodium
intakes and achieved the target sodium intake on placebo,
49 f7 mmol/day. When slow sodium tablets (100 mmol/
day) were given the 24 h urinary sodium excretion
increased to a mean of 155 k 18 mmol/day, significantly
greater ( P < O . O O l ) than on placebo. Body weight on
placebo was 70.9 f 1.8 kg, which was not different from
the value of 71.4 f 1.6 on slow sodium tablets. Resting
blood pressures were similar after 2 weeks on the two
diets [CON= 129/66 mmHg (17.2/8.8 kPa), LOW= 123/
6 3 mmHg (16.4/8.4 kPa)J. The effects of 100 mmol of
sodium/day on baseline variables are summarized in
Table 1.
Table 1. Baseline variables after 2 weeks on either a normal (CON) or reduced (LOW) sodium
intake
Values are means k SEM ( n = 8). Statistical significance: *P<0.05, **P<0.01, ***P<0.001
compared with CON. Blood pressure: to convert mmHg to kPa, divide by 7.5.
CON
Body weight (kg)
Heart rate (beats/min)
Blood pressure (mmHg)
Systolic
Diastolic
Urine electrolytes (mmol/day)
Sodium
Potassium
Chloride
Creatinine
Urea
Plasma electrolytes (mmol/l)
Sodium
Potassium
Chloride
Creatinine
Urea
Plasma osmolality (mosmol/kg)
Plasma renin activity(pmo1of ANG I h - ' ml-I)
Plasma aldosterone (pmol/l)
LOW
71.4k 1.6
59-13
70.9 k 1.8
64+4*
129k4
66-13
123-14
63+3
155+ 18
83-19
159k 16
14.5 k 0.8
380 k 27
49 7***
9 4 k 13
63 k 5***
15.1 -1 1.2
354 -1 35
+
138.6 0.4
4.0k0.1
102.8 k 0.8
0.09 k 0.001
5.8 k 0.5
275k 1
1.5 k 0.2
277 f 36
+
139.3 k 0.5
4.0-10.1
100.4 f 0.6
0.10 -10.00 1
5.6 k 0.5
275 k 2
2.6 k 0.2***
780 k 144**
Sodium intake and exercise-heat tolerance
The subjects reported no side effects on either diet and
did not complain of any tiredness or lethargy while on the
reduced sodium intake. All subjects were able to
complete the full 60 min of exercise in the heat on both
low and normal sodium intakes. Oxygen uptake
(CON=2.30f0.14 l/min, LOW=2.35+0.12 I/min),
heart rate (CON = 158 f5 beats/min, LOW= 161 f3)
and rectal temperature (CON = LOW= 38.0 fO.l°C)
during exercise were similar on the two sodium intakes.
Body weight loss during exercise was similar on the two
diets (CON= 1.27 f 0.1 1 kg, LOW= 1.26 f0.09 kg).
There were no differences between diets in plasma
sodium or potassium either before or during exercise (Fig.
1).The exercise-heat exposure resulted in significant elevations in these plasma electrolytes, the greater being in
potassium. The concentration of sodium in the sweat on
the low sodium intake (38.4k5.2 mmol/l) was lower
(P<0.01) than the corresponding value of the normal
sodium intake (49.7 f 4.3 mmol/l). The concentration of
potassium in the sweat did not differ between diets (Table
2). The sweat rate, estimated from the body weight loss
corrected for respiratory and metabolic water losses, did
not differ between the two diets (Table 2); however, the
amount of sodium lost during exercise on the low sodium
intake was lower than on the normal sodium intake
(Table 2).
Plasma aldosterone was higher at rest after 2 weeks on
a low sodium intake (LOW=780+ 144 pmol/l,
CON = 277 k 36 pmol/l, P< 0.01) and remained so
during exercise (Fig. 2). Plasma r e i n activity demonstrated a similar pattern with both resting
[LOW=2.6+0.2 pmol of angiotensin I (ANG I) h-'
ml-l, CON=1.5+0.2 pmol of ANG I h-I ml-l
P<O.OOl] and exercise levels being higher after 2 weeks
on the low sodium intake (Fig. 2).
Maximal exercise performance was similar on the two
diets, being unaffected by the level of sodium intake.
There were no differences in either peak power
(LOW= 926 f 50 W, CON = 974 f38 W) or total work
(LOW= 2 1.2 k 1.1 kJ, CON = 21.6 f0.8 kJ).
DISCUSSION
In the present study the exercise workloads and the
environmental conditions did not differ for the two levels
of sodium intake. Exercise-heat tolerance was assessed by
555
the physiological response to the combined exercise and
heat stress under these standardized conditions, i.e. an
exaggerated heart rate and rectal temperature response or
an inability to complete the 60 min of exercise after the
reduced sodium intake would indicate impaired exerciseheat tolerance. All subjects completed the full 60 min of
exercise on both diets and there were no differences in
142 1
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0
I
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15
30
60
Exercise time (min)
Fig. 1. Plasma sodium and potassium before and during
exercise in the heat after 2 weeks on either a normal
(CON, 0 ) or reduced (LOW, 0)sodium intake. Values are
means fSEM (n= 8). No differences were seen between
trials; however, all exercise values were higher (P<0.05)
than the respective value before exercise.
Table 2. Sweat rate and composition during exercise after 2 weeks on either a normal (CON) or
reduced (LOW) sodium intake
Values are means f SEM (n= 7). Statistical significance: *P<0.01, **P< 0.001, compared with
CON.
CON
~~
LOW
~
Estimated sweat rate (I/h)
Sweat sodium (mmol/l)
Sodium loss (mmol/h)
Sweat potassium (mmol/l)
Potassium loss (mmol/h)
1.15 f 0.1 1
49.7f 4.3
54.8f 2.9
3.7f 0.4
4.2f 0.5
1.12 f 0.09
38.4f5.2*
40.6 3.6**
4.0f 0.3
4.5f 0.6
*
M. Hargreaves et al.
556
T
*
*
, ***
$/f
d
6
although plasma volume was not measured, the similarity
in body weights before exercise suggests that the hydration state of the subjects was similar on the two sodium
intakes. It has been reported that severe salt restriction in
rats increases the risks associated with certain kinds of
stress (e.g. trauma, haemorrhage) by modifying cardiovascular and sympathetic function [14]. In the present
study, we observed no differences in the heart rate
response to exercise between diets. Furthermore, the level
of sodium restriction was fairly modest (50 mmol/day).
Perhaps more severe sodium restriction would produce
the negative effects that have been observed in rats.
A potential limitation in the present study may be the
inability to detect differences between diets with a
relatively small sample size ( I I = 8). The differences
between the diets for maximal heart rate and rectal temperature were 3.75 f2.8 beats/min and 0.08 0.09”C
(mean fSEM), respectively. With 80% power these differences would have been as high as 7 beats/min and
0.22”C, these values being 4% and O.6%, respectively, of
the observed maximal responses. Thus, if there were differences in responses betweeen diets in the present study
they were probably minor and of little physiological significance.
Plasma renin activity and aldosterone levels were
higher after the low sodium intake and increased during
the exercise-heat exposure in both trials (Fig. 2), the
increases being similar in magnitude to those previously
reported for an equivalent exercise-heat stress [15]. The
exercise-induced increase in plasma renin activity is
closely related to the enhanced sympathoadrenal activity
during exercise [ 161, although alterations in plasma
volume and osmolality may also be important [17]. It has
been shown that plasma renin activity during exercise can
be influenced by the level of dietary sodium [18, 191; a
similar result was obtained in the present study (Fig. 2).
The increase in angiotensin I1 levels [ 191, resulting from
an increase in renin activity, is a major stimulus for aldosterone secretion during exercise [ 191, but increases in
plasma potassium (Fig. 1) and adrenocorticotropic
hormone levels are also likely to be involved in stimulating aldosterone release. The absolute increase in plasma
aldosterone during exercise (CON = 1.227f 175 pmol/l,
LOW=2325+336 pmol/l) and the slope of the aldosterone-time relationship were greater ( P < 0.05) on the
reduced sodium intake. Previously, in humans, it has been
demonstrated that the stimulatory effect of angiotensin I1
on aldosterone release is attenuated with increasing
dietary sodium intake [ 191. Furthermore, sodium restriction alters the adrenal sensitivity and response to angiotensin I1 stimulation [20].The results of the present study
are in line with these observations. Another. hormone that
may be important is antidiuretic hormone. In the present
study there were no differences in plasma osmolality
either before or during exercise. Since the increase in
plasma antidiuretic hormone levels during exercise is
closely related to the increase in plasma osmolality [ 171, it
is likely that antidiuretic hormone levels during exercise
on the two diets were similar. Furthermore, a previous
study has shown little effect of sodium depletion, more
*
32220
3301
t
1
I
1
0
15
30
60
Exercise time (min)
Fig. 2. Plasma renin activity (PRA) and plasma aldosterone concentration (PAC) before and during exercise
in the heat after 2 weeks on either a normal (CON, 0 ) or
reduced (LOW, 0)sodium intake. Values are means fSEM
( n= 6-8). Statistical significance: *P<O.O5, **P< 0.01,
***P<0.001, compared with CON.
exercise heart rates or rectal temperatures between trials.
Thus, it appears that moderate salt restriction did not
impair exercise-heat tolerance. Recently it has been
demonstrated that the process of heat acclimatization in
man is unaffected by the level of dietary sodium [lo].
Furthermore, rats placed on an extremely sodiumdeficient diet did not exhibit circulatory hyponatraemia or
decrements in endurance exercise performance in the
heat [12]. These authors suggested that the hormonal
responses to the low sodium intake were important in
maintaining plasma sodium levels and exercise performance. In the present study there were no differences in
plasma sodium either before or during exercise (Fig. 1)
despite the threefold difference in dietary sodium intake,
most likely the result of the increases in plasma renin
activity and aldosterone (Fig. 2). Two important factors
influencing thermal balance during exercise are plasma
volume and osmolality [ 131. In the present study no differences in plasma osmolality were observed between
diets either before or during exercise. Furthermore,
Sodium intake and exercise-heat tolerance
severe than in the present study, on plasma antidiuretic
hormone levels 1211.
It has been suggested that alterations in sodium intake
may influence the intracellular calcium level in vascular
smooth muscle cells and, as a result, the blood pressure
[22]. Thus, an increase in sodium intake ultimately leads
to an increase in intracellular calcium in smooth muscle
and a more forceful contraction when stimulated [22].It is
presumed that a reduction in sodium intake results in an
opposite effect [22]. Whether such a mechanism operates
in skeletal muscle, where intracellar calcium is well
buffered by the sarcoplasmic reticulum, is speculation.
Nevertheless, we though it of interest to examine whether
a reduction in sodium intake had any negative effect on
muscle performance during maximal dynamic exercise.
While there was no differencebetween diets in total work
output during maximal exercise, peak power was slightly
lower (P=O.lO) after 2 weeks on the reduced sodium
intake. Thus, the effect of alterations in sodium intake on
muscle performance may warrant further investigation.
The results of the present study indicate that moderate
dietary sodium restriction does not impair the ability to
exercise in a hot environment and infer that advice to
reduce salt intake can be given safely.
ACKNOWLEDGMENTS
We thank Rosemary Snowden, Caryl Nowson and Janet
Cripps for their assistance during this study. M.H. was
supported by the National Health and Medical Research
Council of Australia.
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